Fetotoxicity caused by the interaction between zinc and arsenic in mice.

Maria Luiza Fascineli, E Sidney Hunter, Wilma De Grava Kempinas
{"title":"Fetotoxicity caused by the interaction between zinc and arsenic in mice.","authors":"Maria Luiza Fascineli,&nbsp;E Sidney Hunter,&nbsp;Wilma De Grava Kempinas","doi":"10.1002/tcm.10026","DOIUrl":null,"url":null,"abstract":"<p><p>Arsenic is an environmental pollutant that induces congenital malformations in experimental models and can contribute to human birth defects. The environmental exposure to arsenic is relatively small when compared with the doses required to cause teratogenicity in mice and other laboratory animals. In order to study the action of zinc in the arsenic-induced teratogenicity, in the present work mice were either pretreated with zinc and later with arsenic or were treated simultaneously with zinc and arsenic in vivo and in vitro. Following administration of arsenate on gestation day 8, pregnant females were killed on the 17th day of gestation; maternal and fetal data were collected by laparotomy and used to calculate reproductive parameters. Fetuses were analyzed for the presence of external malformation and, after the appropriate processing, visceral and skeletal analyses were accomplished. Conceptuses were exposed in whole embryo culture to arsenicals on gestation day 8 (3-6 somite stage). After a 26 h culture period, morphological development was assessed. Neither pretreatment with zinc nor simultaneous administration of zinc prevented arsenic teratogenicity in these experimental models.</p>","PeriodicalId":22336,"journal":{"name":"Teratogenesis, carcinogenesis, and mutagenesis","volume":"22 5","pages":"315-27"},"PeriodicalIF":0.0000,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/tcm.10026","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Teratogenesis, carcinogenesis, and mutagenesis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/tcm.10026","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 10

Abstract

Arsenic is an environmental pollutant that induces congenital malformations in experimental models and can contribute to human birth defects. The environmental exposure to arsenic is relatively small when compared with the doses required to cause teratogenicity in mice and other laboratory animals. In order to study the action of zinc in the arsenic-induced teratogenicity, in the present work mice were either pretreated with zinc and later with arsenic or were treated simultaneously with zinc and arsenic in vivo and in vitro. Following administration of arsenate on gestation day 8, pregnant females were killed on the 17th day of gestation; maternal and fetal data were collected by laparotomy and used to calculate reproductive parameters. Fetuses were analyzed for the presence of external malformation and, after the appropriate processing, visceral and skeletal analyses were accomplished. Conceptuses were exposed in whole embryo culture to arsenicals on gestation day 8 (3-6 somite stage). After a 26 h culture period, morphological development was assessed. Neither pretreatment with zinc nor simultaneous administration of zinc prevented arsenic teratogenicity in these experimental models.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
小鼠锌和砷相互作用引起的胎儿毒性。
砷是一种环境污染物,在实验模型中引起先天性畸形,并可能导致人类出生缺陷。与在小鼠和其他实验动物中引起致畸所需的剂量相比,砷的环境暴露相对较小。为了研究锌在砷致致畸中的作用,本研究在体内和体外分别采用先锌后砷或同时锌和砷处理的方法。妊娠第8天给予砷酸盐,妊娠第17天处死母鼠;通过剖腹手术收集母胎资料,计算生殖参数。分析胎儿是否存在外部畸形,并在适当处理后,完成内脏和骨骼分析。妊娠第8天(3 ~ 6个月)全胚暴露于砷环境中。培养26 h后,观察其形态发育情况。在这些实验模型中,锌预处理和同时给锌都不能防止砷致畸。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Differential toxic effect of cis-platinum(II) and palladium(II) chlorides complexed with methyl 3,4-diamine-2,3,4,6-tetradeoxy-alpha-L-lyxo-hexopyranoside in mouse lymphoma cell lines differing in DSB and NER repair ability. Differential role of hydrogen peroxide and organic hydroperoxides in augmenting ferric nitrilotriacetate (Fe-NTA)-mediated DNA damage: implications for carcinogenesis. Inhibitory effect of Eucommia ulmoides Oliv. on oxidative DNA damage in lymphocytes induced by H2O2. Expression of aphidicolin-induced fragile sites and their relationship between genetic susceptibility in breast cancer, ovarian cancer, and non-small-cell lung cancer patients. Mutant spectra analysis at hisG46 in Salmonella typhimurium strain YG1029 induced by mammalian S9- and plant-activated aromatic amines.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1